Informace o publikaci

Hematopoiesis of mouse embryonic stem cells – the role of p38alpha kinase

Název česky Hematopoéza myších embryonálních kmenových - role p38alfa kinázy


Rok publikování 2013
Druh Další prezentace na konferencích
Fakulta / Pracoviště MU

Přírodovědecká fakulta

Popis Hematopoietic differentiation of embryonic stem cells (ESCs) in vitro has been used as a model to study early hematopoietic development. Identifying the molecular pathways regulating hematopoietic stem cell (HSC) or hematopoietic progenitor cell (HPC) specification, self-renewal, and expansion remains a fundamental goal of both basic and clinical biology. Similarly to the other members of MAPK family, p38 signaling is involved in plenty of cell responses from cell cycle to apoptosis, induction of cytokine genes, and differentiation. Recently, it has been shown that MAPK p38alpha plays a role in regulation of adult hematopoiesis, particularly erythropoiesis and granulopoiesis (Geest C.R., Coffer P.J., 2009). Besides MAPK signaling has been demonstrated to play a key role in the maintenance of HSC quiescence (Ito K. et al, 2006). The aim of our work was to study the mechanisms and effectiveness of hematopoiesis in mouse ES cells, in consideration of mitogen-activated protein kinase (MAPK) p38. We suppose that if p38alpha kinase participates on the maintenance of the hematopoietic stem and early progenitor cells, depletion of p38alpha kinase changes the dynamics of hematopoiesis in p38alpha -/- when compared to the wildtype p38 ES cell line. So during differentiation of mentioned ES cells we determined dynamic of hematopoiesis using qRT-PCR, colony-forming assay and FACS phenotyping. Our results show that both p38alpha +/+ and p38alpha -/- cells are able to be directed to hematopoietic cell lineages. However p38alpha deficient cells undergo hemasopoiesis more intensively in contrast to their wild-type counterpart. P38alpha -/- cells also in higher ration form/create erythroid and granulopoietic lineages. In contrast, wild-type cells are able to better maintain CD34 positive cell sub-population. Thus based on our preliminary data we can hypothesize that depletion of p38alpha MAPK leads both to attenuating stemness and to enhancing myeloid progenitors development.